MAF (MAF BZIP Transcription Factor)

Flow cytometry demonstrated an alteration in the proportion of immune cells in Mtb-infected mouse lungs due to Mafb deficiency. Together, Mafb in myeloid cells is involved not only in the functional antibacterial process of macrophages but also in immune cell recruitment in the lungs, thereby contributing to host defense against Mtb infection.

The case is the first known report of liver disease in the setting of germline MAF variants. It implicates LSEC dysfunction in both non-neoplastic and neoplastic liver disease and lends insight into the importance of LSECs in liver health and homeostasis.

Our findings indicate that soluble LOX secreted by CAFs promotes metastatic progression through the induction of pulmonary fibrosis. Targeting this LOX-mediated pathway may represent a promising therapeutic strategy for preventing lung metastasis in patients with SACC. Furthermore, given the complexity of metastasis, future studies should investigate how fibrosis influences key stages of metastatic colony formation, including the extravasation and dormancy of circulating tumour cells.

Clinical sample analysis confirmed elevated p-STAT3 and c-MAF expression in IL-6R+CD8+ T cells, correlating with increased exhaustion. These findings suggest that CD8+ T cell-based risk models may serve as effective prognostic tools in HCC and that targeting the IL-6/STAT3 axis represents a promising immunotherapeutic strategy.

Finally, in vivo studies indicated that M. tuberculosis-mediated increase of MafB expression was responsible for the exacerbation of M. tuberculosis infection. Thus, our results provide a functional view of MafB as a cytokine regulator as well as novel insights into host factors involved in TB susceptibility.

Adjuvant bisphosphonate therapy, like zoledronic acid (ZOL), is recommended for postmenopausal women with early-stage breast cancer to lower bone metastasis risk and improve survival...Although initial testing costs are involved, long-term benefits from reduced recurrence and adverse outcomes suggest a favorable budget impact beyond 10 years. These findings support integrating MAF testing into clinical practice to enhance both clinical efficacy and cost-efficiency in breast cancer care.

These observations suggested that RICs-MAF might have experienced a non-canonical multipotent state during lineage conversion. In sum, we report a unique approach of an exo-ribosome-mediated plastic state of MAF that is amenable to multi-lineage conversion.

AANAT1 knockout/knockdown insects were more susceptible to insecticide treatments. Our study reveals that normal functionality of AANAT1 is important for the regulation of gut detoxification pathways, providing insights into the mechanism underlying the gut defense against xenobiotics in metazoans.

In ROS scavenger assays, it was found that the expression of CncC/Maf significantly decreased, along with a decrease in the ABC transporter genes. The present study showed that beta-cypermethrin seemed to trigger the outbreak of ROS, subsequently activated the CncC/Maf pathway, as a result induced the ABC transporter-mediated resistance to the drug, shedding more light on the resistance mechanisms of D.gallinae to pyrethroids.

Additionally, this approach led us to identify a series of potential new targets for MM patients, depicting a new scenario where each patient could be “screened” to identify the best molecule to be targeted. While further investigation is necessary to assess off-target toxicity and confirm clinical relevance, our analyses significantly streamline the search for tumor markers with a method potentially applicable to different malignancies, bringing us closer to identifying the best candidates for effective CAR therapy.

Six compounds were selected for further experimental assay: vemurafenib, sorafenib, sildenafil, fluvastatin, erlotinib, and glimepiride. Moreover, both compounds simultaneously downregulated c-Maf protein expression to induce G1 phase arrest and apoptosis in myeloma cells. Collectively, sorafenib and glimepiride may be considered promising candidates for developing more potent c-Maf inhibitors in the future.

Importantly, these molecules target c-Maf-expressing multiple myeloma cells, but not c-Maf-negative myeloma cells, showing potential for tailoring therapeutic intervention. In conclusion, our screening pipeline is effective to explore leads for a novel c-Maf inhibitor for multiple myeloma therapy.